Onset of psoriasis in patients receiving anti-TNF agents

In the past decade, tumour necrosis factor (TNF) antagonists have been found to be remarkably effective for the treatment of immune-mediated inflammatory disorders such as rheumatoid arthritis and Crohn’s disease. These agents also dramatically lessen inflammation and improve the quality of life in patients with psoriasis and psoriatic arthritis. The TNF-blocking agents have been relatively safe, although some concerns have been raised on the basis of a recent meta-analysis of trial data that identified an increased risk of serious infections and solid malignancy in a small percentage of patients treated with anti-TNF antibodies. Of late, attention has also focused on a wide spectrum of skin lesions arising in patients treated with TNF antagonists. The list is quite extensive, but some of the more common dermatological conditions include skin infections, skin tumours, discoid lupus, eczema, vasculitis and drug-related eruptions. Perhaps one of the most perplexing lesions are the psoriasiform eruptions that have been described in patients with rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease and Behçet’s disease during anti-TNF treatment, particularly because TNF is a pivotal molecule in the pathophysiology of psoriatic skin lesions. To date, 30 cases of psoriasiform skin eruptions have been reported in patients receiving TNF antagonists. Table 1 summarises the demographics and information regarding diagnosis, type of TNF antagonist and details of the appearance and resolution of the skin lesions. Most of the patients had underlying rheumatoid arthritis, although this may simply reflect the fact that more patients with this diagnosis receive treatment with antiTNF agents. Eight patients were receiving treatment for ankylosing spondylitis, two had inflammatory bowel disease and two had Behçet’s disease. The mean age of patients was 49.8 years and disease duration ranged from 5 to 21 years. The most common skin eruption was pustular psoriasis; 10 patients had psoriasis vulgaris, whereas only one patient had the guttate variety, and another had both the guttate and vulgaris forms. Almost half of the patients were taking infliximab, eight were taking adalimumab and eight were taking etanercept. The onset of psoriasis occurred .12 weeks after the TNF antagonists were started in 21 patients, and psoriasis remained active in most of the patients maintained on TNF-blocking agents. When the TNF antagonist was stopped, psoriasiform lesions resolved in four patients and persisted in one. Only 12 patients were receiving concomitant disease-modifying anti-rheumatic drugs, which included leflunomide, sulfasalazine, methotrexate and azathioprine. In all, only eight patients had a personal or family history of psoriasis. Several observations emerge from these data: